Recombinant human growth hormone administered for three months to patients with idiopathic dilated cardiomyopathy increased myocardial mass and reduced the size of the left ventricular chamber, resulting in improvement in hemodynamics, myocardial energy metabolism, and clinical status.

Bariatric surgery is recognized as a highly effective therapy for obesity since it accomplishes sustained weight loss, reduction of obesity-related comorbidities and mortality, and improvement of quality of life. Overall, bariatric surgery is associated with a 42% reduction of the cardiovascular risk and 30% reduction of all-cause mortality. This review focuses on some nutritional consequences that can occur in bariatric patients that could potentially hinder the clinical benefits of this therapeutic option. All bariatric procedures, to variable degrees, alter the anatomy and physiology of the gastrointestinal tract; this alteration makes these patients more susceptible to developing nutritional complications, namely, deficiencies of macro- and micro-nutrients, which could lead to disabling diseases such as anemia, osteoporosis, protein malnutrition. Of note is the evidence that most obese patients present a number of nutritional deficits already prior to surgery, the most important being vitamin D and iron deficiencies. This finding prompts the need for a complete nutritional assessment and, eventually, an adequate correction of pre-existing deficits before surgery. Another critical issue that follows bariatric surgery is post-operative weight regain, which is commonly associated with the relapse of obesity-related co-morbidities. Nu-tritional complications associated with bariatric surgery can be prevented by life-long nutritional monitoring with the administration of multi-vitamins and mineral supplements according to the patient’s needs.

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IntroductionThe reason why hyperinsulinemia is associated with essential hypertension is not known. To test the hypothesis of a pathophysiologic link mediated by the sympathetic nervous system, we measured the changes in forearm norepinephrine release, by using the forearm perfusion technique in conjunction with the infusion of tritiated NE, in patients with essential hypertension and in normal subjects receiving insulin intravenously (1 mU/ kg per min) while maintaining euglycemia.Hyperinsulinemia (50-60 jsU/ml in the deep forearm vein) evoked a significant increase in forearm NE release in both groups of subjects. However, the response of hypertensives was threefold greater compared to that of normotensives (2.28±45 ng. liter-' * min' in hypertensives and 0.80±0.27 ng. liter-' in normals; P < 0.01). Forearm Although the coexistence ofhyperinsulinemia and essential hypertension has long been recognized (1-3), the nature and the significance of this association are far from being completely elucidated. A critical question is whether hyperinsulinemia is causally related to the development of hypertension and, if so, what mechanism underlies insulin action on blood pressure regulation. The question is under active investigation but the data available so far are not entirely consistent. Substantial evidence favoring a causal role of insulin comes essentially from the studies in fructose-fed rats (4-6). In this model, insulin resistance, hyperinsulinemia, and hypertension develop and this sequence may be interrupted by preventing either insulin resistance with physical exercise or hyperinsulinemia with somatostatin (5, 6).The relationship between insulin and human hypertension has been extensively investigated on epidemiological ground, less so from a mechanistic standpoint. The available clinical data, however, tend to support the concept that the two factors must be linked by pathophysiologic mechanisms. Particularly relevant is the observation that a program of physical activity or body weight control leads to a parallel reduction of hyperinsulinemia and blood pressure levels (7). Of interest is also the recent observation that in the offspring of essential hypertensive parents insulin resistance and hyperinsulinemia are demonstrable before the development of high blood pressure (8).Among the various factors considered as potential links between insulin and blood pressure, the sympathetic nervous system is indicated as a prime candidate for a number of reasons: (a) in hypertensive patients, glucose intolerance and insulin resistance with attendant hyperinsulinemia have been amply demonstrated (3, 9, 10); (b) in normal individuals, insulin evokes sympathetic overactivity (1 1, 12); (c) increased sympathetic activity in essential hypertension, particularly in the mild form of young hypertensives, has been documented by a variety of approaches (13,14); and (d) sympathetic overactivity may be potentially responsible for elevated blood pressure (15) and may antagonize insulin action (16)(17)(18)(19)(20). Ba...

Data are expressed as mean 6 SD. *Paired sample t test.

At equivalent glycemic control, rosiglitazone, but not metformin, improves endothelium dependent vasodilatation and insulin sensitivity in type 2 diabetes.

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OBJECTIVETo evaluate whether the high triglyceride-to-HDL cholesterol (TG-to-HDL-C) ratio is associated with cardiometabolic risk (CMR) factors and preclinical signs of organ damage in an outpatient population of white children and adolescents.RESEARCH DESIGN AND METHODSThe study population included 884 subjects (aged 6–16 years), of whom 206 (23%) were normal weight, 135 (15%) were overweight, and 543 (61%) were obese. Biochemical variables were analyzed in the whole sample, whereas homocysteine and left ventricular (LV) geometry and function were evaluated in 536 and 258 children, respectively.RESULTSThe percentage of pubertal children (P < 0.001), as well as measurements of BMI, waist circumference, homeostasis model assessment of insulin resistance, white blood cell count, alanine aminotransferase (ALT), systolic blood pressure (P < 0.0001, for all), creatinine (P < 0.001), and diastolic blood pressure (P < 0.02), increased from the lowest to the highest tertile of the TG-to-HDL-C ratio. Age, sex, homocysteine, and glomerular filtration rate did not change. Moreover, interventricular septum thickness, relative wall thickness, and LV mass index (P = 0.01 to P < 0.0001) increased across tertiles of the TG-to-HDL-C ratio. Children with a TG-to-HDL-C ratio ≥2.0 showed a two- to threefold higher risk of elevated ALT levels and concentric LV hypertrophy than those with a TG-to-HDL-C ratio <2.0, independent of confounding factors.CONCLUSIONSThe high TG-to-HDL-C ratio is associated with several CMR factors and preclinical signs of liver and cardiac abnormalities in the outpatient, white pediatric population. Thus, a TG-to-HDL-C ratio ≥2.0 may be useful in clinical practice to detect children with a worsened CMR profile who need monitoring to prevent cardiovascular disease in adulthood.